Test 3: Wk 11: 8 Neural Control of Breathing - Puri Flashcards
Dyspnea is the feeling of
being short of breath, or the unpleasant conscious
awareness of difficulty in breathing.
when arterial PaO2 falls or PaCO2 rises from breath holding, asphyxia,
or pulmonary disease, dyspnea leads to
efforts to increase ventilation and thus to restore arterial blood gas levels to normal
What causes dyspnea when blood gasses are normal
increased airway resistance
mechanical event for inspiration
contraction of diaphragm
neural event for inspiration
firing of phrenic motoneurons
where are phrenic motor neurons located
within the ventral horn of the cervical spinal cord c3-c5
mechanical event for expiration
relaxation of diaphragm and recoil of lungs
neural event for expiration
phrenic motoneurons stop firing
rate of respiration is dependent on
the interval between bursts of phrenic nerve action potentials
tidal volume is determined by
the strength of the diaphragm contraction which is determined by the number of phrenic motor units recruited
— controls the act of breathing
the medullary pattern generator
below level IV
all breathing stops
Below level I
all breathing intact
cut at level III (btwn pons and medulla)
tidal volume increased and apneustic breathing starts
Dorsal Respiratory Group (DRG are — neurons in the —
Inspiratory neurons in the ventrolateral nucleus of the tractus solitarius (NTS)
The tractus solitarius project primarily to the — for —
contralateral phrenic motoneurons for passive inspiration and expiration
expiratory neurons in the nuclease retroambigualis
Ventral Respiratory Group (VRG)
the nucleus retroambigualis project to — and — for —
contralaterally to abdominal and intercostal muscles.
Primarily for forced expiration
Bötzinger and Pre-Bötzinger complexes contain
pacemaker cells
for automatic generation of respiratory rhythm
Inspiratory “Ramp” Signal:
The nervous signal that is transmitted to the inspiratory
muscles, mainly the diaphragm via the phrenic nerve
how does ramp signal work
not an instantaneous burst of action potentials. Instead, it begins weakly and increases steadily in a ramp manner for about 2 seconds in normal respiration. Then it ceases abruptly for approximately the next 3 seconds, which turns off the excitation of the diaphragm and allows elastic recoil of the lungs and the chest wall to cause expiration.
advantage of ramp signal
causes a steady increase in the volume of
the lungs during inspiration, rather than inspiratory gasps
The — controls the “switch-off” point of the inspiratory ramp, thus
controlling the duration of the filling phase of the lung cycle.
pneumotaxic center
The function of the pneumotaxic center is primarily —
to limit inspiration
apneustic breathing
prolonged inspiratory efforts interrupted by
occasional expirations
opiates inhibit
the central pattern generator
opiates and benzos cause
respiratory depression
Excitatory amino acids, —, activated — receptors
glutamate, NMDA
Inhibitory neurotransmitters include — and —
glycine and γ-aminobutyric acid (GABA)
Benzodiazepines exert their
effect by binding directly to — increasing the inhibitory effect
of —
GABAA
endogenous GABA.
Peripheral chemoreceptors activate the CPG via
glutamate-releasing neurons.
Central chemoreceptors activate the CPG via
acetylcholine-releasing neurons.
peripheral chemoreceptors located in
carotid bodies and aortic bodies
Peripheral chemoreceptors carotid bodies afferent pathway
Glossopharyngeal Nerve CN IX
Peripheral Chemoreceptor aortic bodies afferent pathway
Vagus Nerve CN X
peripheral chemoreceptors are exposed to
arterial blood
peripheral chemoreceptors respond to (3)
⬇ PaO2
⬆ PaCO2
⬇ pH
peripheral chemoreceptors pH detected by — only
carotid
central chemoreceptors location
ventrolateral medulla near exits of CN IX and X
central chemoreceptors chemical stimuli
increased medullary extracellular and CSF H+ resulting from ⬆ PaCO2
central chemoreceptors are not stimulated by
decreased PO2 (hypoxia)
central chemoreceptors respond to changes in — H+ concentration
CSF
— ions directly activated central chemoreceptors
H+
— does not directly act on central chemoreceptors
CO2
normal drive for ventilation during acute hypercapnia
increased PaCO2
— are acute regulators of day to day breathing and respond to changes in —
central chemoreceptors
CO2
defect in central chemoreceptors
they “reset” if changes in CO2 are prolonged, like baroreceptors
shift in sensitivity to PaCO2 is exaggerated in
metabolic acidosis
Chemical control of breathing in pts with chronic hypercapnia
central chemoreceptors adapt to prolonged elevated PaCO2 and are no longer the central regulator
pts with COPD have decreased O2 which will activate peripheral chemoreceptors
the main stimulus to breathe in chronic hypercapnia is
Hypoxic Drive
oxygen induced hypoventilation
administration of high concentrations of O2 to a person with chronic hypercapnia will increased their Pa)2 and knock out their hypoxic drive
for hypoxic drive to kick in PaO2 must drop below
60mmHg
when PaO2 decreases to threshold levels the ventilatory response is mediated solely by
carotid chemoreceptors
— does not stimulate the central chemoreceptors
decreased PaO2
synergistic effect on ventilation when
increased PaCO2 accompanies decreased PaO2
pulmonary stretch receptors act to
terminate inspiration and decrease respiratory rate by increasing expiratory time
Hering-Breuer Inflation Reflex mediated by
impulses traveling in the vagus nerve
Hering-Breuer Inflation Reflex originates in slowly adapting stretch receptors located within
smooth muscle of large bronchi and small bronchioles
most stretch receptors fire during
tidal breathing
deep breaths — Liter(s) are sufficiently large enough to trigger stretch reflex
1 liter
Activation of rapidly adapting receptors in the trachea cause
cough, bronchoconstriction, and mucus secretion
